Prevention Of Fetal Growth Restriction Research Articles

Recombinant vascular endothelial growth factor 121 injection for the prevention of fetal growth restriction in a preeclampsia mouse model

To discover the potential role of recombinant VEGF121 (rVEGF121) injection for the prevention of fetal growth restriction in a preeclampsia (PE) mouse model (Mus musculus). This is an experimental study of 30 pregnant mice that were randomly divided into three groups: normal, PE, and PE with rVEGF121 injection. The PE mouse model was created by injecting anti Qa-2 10 ng iv, which is deleterious to Qa-2 expression (homologous to HLA-G), from the first to the fourth day of gestation. PE was validated by measuring serum levels of soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor(PIGF) and also by kidney histopathology. Recombinant VEGF121 was given on the ninth day until the 11th day of pregnancy; mice were terminated on the 16th day. Fetal weights were acquired with a Denver analytical balance. Serum levels of sFlt-1 and PlGF were measured using enzyme-linked immunosorbent assay (ELISA). The data were statistically analyzed via analysis of variance (ANOVA). On average, fetal birth weight was 0.7150 g in the normal group, 0.4936 g in the PE group, and 0.6768 g in the PE with rVEGF121 injection group. ANOVA showed significant growth restriction in the PE group (P=0.006), confirming the use of anti Qa-2 as a suitable PE model. Kidney histopathology results, sFlt-1 levels, and PlGF levels also demonstrated that anti Qa-2 consistently conferred hallmarks of PE in mice. Vascular endothelial growth factor (VEGF) injection prevented fetal growth restriction; comparable fetal weights were observed between the PE model with VEGF treatment and the normal group (P=0.610) but differed from the untreated PE group (P=0.021). Injection of rVEGF121 has the potential to prevent fetal growth restriction in a newly proposed PE mouse model.

Роль детоксикационной терапии в профилактике задержки роста плода

The objective of the study was to evaluate the efficacy of detoxification therapy omega-3-polyunsaturated fatty acids and flower pollen (apifitohol) in fetal growth restriction prevention (FGR). In the 1st trimester of pregnancy 140 pregnant women were randomized to receive omega-3-PUFA (group 1), apifitohol (group 2) or no treatment group (group 3). In the beginning of the pregnancy and 1st day after labor all patients passed daily urine Pb/Cd test, and benz(a)pyrene/styrene/formaldehyde blood serum test. The patients of the 1st and 2nd group had much lower level of heavy metals in daily urine and organic pollutants in blood serum after labor compared with the onset of pregnancy. FGR was twice more often, and newborn weight was significantly lower in women of no treatment group ( p=0,0022). Detoxification therapy during the pregnancy can prevent FGR and can be recommended in the condition of environmental pollution.

Guest editorial: Fetal growth restriction and its consequences

Worldwide, more than 30 million infants are born with low birth weight each year. India contributes the lion’s share with more than 8 million low weight births annually. A majority of these are born at term but have experienced fetal growth restriction. While a proportion of these cases can be ascribed to recognizable etiological mechanisms, such as maternal malnutrition, systemic illness or pregnancy related complications, no definite cause can be ascertained in a vast majority. These infants are at increased risk of mortality and morbidity in early life; as well as a greater later risk of developing central obesity, dyslipidemia, hypertension, insulin resistance and diabetes, as well as short stature and early puberty. Over the past many years, research efforts to elucidate the biology of normal and abnormal growth have not been commensurate with the magnitude of the problem. There has been a paucity of novel/path-breaking research for identification of underlying mechanistic pathways as well as successful interventions for prevention of fetal growth restriction and its adverse consequences. However, with recent technological advances in the understanding of genetic/ epigenetic pathways and availability of sophisticated bioinvestigation tools, there is an opportunity to make renewed research efforts in this direction. An international scientific meeting titled “Consultation on Biology of Fetal Growth Restriction and its Consequences” was organized at the All India Institute of Medical Sciences, NewDelhi from 23rd to 25th November, 2010, with the aim to review the current status of research, and to define and prioritize research ideas in this field. The meeting saw active participation by experienced researchers, policy-makers and funding agencies, including National Institute of Health, USA, Indo-US Science and Technology Forum, and the Departments of Biotechnology and Health Research of Government of India. The deliberations of this meeting included wide-ranging discussions on themes such as role of endocrine pathways and one carbon metabolism in regulation of fetal growth, effect of maternal micronutrient deficiency/supplementation on growth and metabolism in the offspring, the ‘omics’ approach to explore pathways of fetal growth restriction, developmental programming of body composition, and the potential mechanisms underlying developmental origins of diseases. The most important recommendations that emerged from the meeting were that there is an urgent need to conduct cohort studies to a), identify fetal growth patterns and determinants of fetal growth restriction in different populations and b), to prospectively study early growth trajectories of small for gestational age infants in resource-limited settings to identify growth patterns that optimize the risk to benefit balance in terms of stature, body composition, risk of infections, undernutrition, later cardiovascular/diabetes risk and neuro-cognitive development. It was felt that India, with its high burden of fetal growth restriction, a population in transition (economic, nutritional and socio-demographic), tremendous science capacity as well as enhanced budgetary allocation for health research by the Government, is uniquely poised to undertake significant research in this field. V. Jain Division of Pediatric Endocrinology, Department of Pediatrics, All India Institute of Medical Sciences, New Delhi, India e-mail: drvandanajain@gmail.com

Guidelines on the investigation and management of antiphospholipid syndrome

This guidance updates and replaces the previous guideline on the investigation and management of antiphospholipid syndrome (APS) published in 2000 (Greaves et al, 2000), though where there have not been changes we refer back to them when appropriate. The guidance is updated with reference to relevant publications since 2000. Publications known to the writing group were supplemented with additional papers identified by searching PubMed for publications in the last 11 years using the key words: lupus anticoagulant, anticardiolipin, antiphospholipid, b2–glycoprotein I, antiprothrombin and limits (clinical trial, randomized control trial, meta-analysis, humans, core clinical journals, English language). The writing group produced the draft guideline, which was subsequently revised by consensus by members of the Haemostasis and Thrombosis Task Force of the British Committee for Standards in Haematology. The guideline was then reviewed by a sounding board of approximately 50 UK haematologists, the Royal College of Obstetricians and Gynaecologists (RCOG), and the British Committee for Standards in Haematology (BCSH) Committee and comments incorporated where appropriate. The ‘GRADE’ system was used to quote levels and grades of evidence, details of which can be found at http://www.bcshguidelines.com/BCSH_PROCESS/EVIDENCE_LEVELS_AND_GRADES_OF_RECOMMEN DATION/43_GRADE.html. The objective of this guideline is to provide healthcare professionals with clear guidance on the diagnosis and management of patients with antiphospholipid syndrome though individual patient circumstances may dictate an alternative approach.

Effects of metformin use in pregnant patients with polycystic ovary syndrome

Use of metformin throughout pregnancy in women with polycystic ovary syndrome (PCOS) has shown to reduce the rates of early pregnancy loss, preterm labor, and prevention of fetal growth restriction. Metformin has been shown to have encouraging effects on several metabolic aspects of polycystic ovarian syndrome, such as insulin sensitivity, plasma glucose concentration and lipid profile and since women with PCOS are more likely than healthy women to suffer from pregnancy-related problems like early pregnancy loss, gestational diabetes mellitus and hypertensive states in pregnancy, the use of metformin therapy in these patients throughout pregnancy may have beneficial effects on early pregnancy loss and development of gestational diabetes.

An economic evaluation of alternative test-intervention strategies to prevent fetal growth restriction in singleton pregnancies

AimTo investigate the potential cost-effectiveness of alternative ‘test and treat’ strategies in the prevention of fetal growth restriction compared to a strategy of no screening in the UK.MethodsEconomic evaluation using...

The Cohen diabetic rat as a model for fetal growth restriction: Vitamins C and E reduce fetal oxidative stress but do not restore normal growth

Fetal growth restriction (FGR) describes newborns that were born small for gestational age. The etiology of FGR is unknown, but it is assumed that it is the consequences of both genetic and environmental factors, and that one of the important environmental factors is oxidative stress. In this study we used the Cohen diabetic (CD) rats (sensitive and resistant strains) and the original Sabra strain fed either high sucrose low copper diet-HSD or regular diet-RD to evaluate the genetic and environmental factors contributing to FGR. In addition, we treated the pregnant rats with antioxidants (vitamins C and E added to their food) to evaluate the effects of antioxidants in the prevention of FGR and in changing the redox state of the fetuses. Methods The study was performed on term 21-day-old fetuses of the three strains fed RD or HSD. Fetal and placental weight and fetal crown rump length were measured. Heart, kidneys, brain and liver were also weighted and studied. The fetal and placental redox status was investigated by studying the levels of Malondialdehyde (MDA) to determine the lipid peroxidation damage and by measuring the activity of catalase (CAT) and superoxide dismutase (SOD) enzymes. Similar studies were performed following the addition of 0.1% of vitamins C and E to the diet. Results FGR in the Cohen diabetic rats is a consequence of genetic (6–20% reduction in fetal weight in the CDr and CDs compared to Sabra) and environmental (11–36% reduction in fetal weight while on HSD) factors, with greater susceptibility in the CDs diabetic rats. Increased lipid peroxidation was observed in some of the organs only in HSD, however not only in the sensitive strain. In each organ, different patterns of anti oxidant capacity were observed. The addition of antioxidants to the food significantly reduced the signs of enhanced oxidative stress in all animals but partially restored normal fetal growth only in the diabetic CDs rats. This may imply that in this model oxidative stress is apparently not a major contributor to FGR. Conclusions Cohen diabetic rats are a good model for the study of the interaction of genetic and environmental factors in the development of FGR. Maternal nutrition can influence the antioxidant capacity of the fetal organs which is modified by antioxidants. However, FGR in our model does not seem to result primarily from enhanced oxidative stress, as it is only partially affected by the antioxidant treatment. Thus, the repeated observations of oxidative stress in SGA infants may be a resulting metabolic alteration of FGR and not the main cause.